Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Cancer progression and p53

D A Carson1, A Lois

  • 1Sam and Rose Stein Institute for Research on Aging, University of California, San Diego, La Jolla 92093-0663, USA.

Lancet (London, England)
|October 14, 1995
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Comparison of Histopathologic Features of Right and Left Sided Colon Cancer.

ANZ journal of surgery·2026
Same author

2-Chlorodeoxyadenosine (2-CdA): A Potent Chemotherapeutic and Immunosuppressive Nucleoside.

Leukemia & lymphoma·2016
Same author

Immunoglobulin Gene Rearrangement and Expression in B-CLL.

Leukemia & lymphoma·2016
Same author

2-Chlorodeoxyadenosine Treatment of Refractory Chronic Lymphocytic Leukemia.

Leukemia & lymphoma·2016
Same author

Genetic and epigenetic profiling of CLL disease progression reveals limited somatic evolution and suggests a relationship to memory-cell development.

Blood cancer journal·2015
Same author

Lymphocyte dysfunction caused by deficiencies in purine metabolism.

Immunology today·2014

Somatic cells face selection pressures that can lead to cancer. The p53 gene, a guardian of the genome, prevents this by controlling DNA repair and cell death, but its disabling mutations in tumors lead to aggressive disease.

Area of Science:

  • Genetics
  • Molecular Biology
  • Cancer Research

Background:

  • Somatic cells in complex organisms are subject to selection pressures, favoring mutants that survive environmental insults and proliferate autonomously.
  • Uncontrolled mutation, selection, and proliferation cycles can drive malignant transformation and lead to cancer.
  • Organisms possess intrinsic mechanisms to prevent cancer, including accurate DNA repair, programmed cell death for damaged cells, and limited replicative lifespans.

Purpose of the Study:

  • To highlight the critical role of the p53 gene as a "guardian of the genome" in preventing cancer.
  • To elucidate the functions of p53 in DNA damage response and cellular senescence.
  • To underscore the implications of p53 dysfunction in human tumorigenesis.

Main Methods:

Related Experiment Videos

  • The abstract does not detail specific experimental methods but discusses biological processes and genetic observations.
  • It focuses on the regulatory functions of the p53 gene in cellular responses to DNA damage.
  • It reviews the frequency and consequences of p53 mutations in human cancers.

    • Main Results:

    • Disabling mutations and deletions of the p53 gene are found in approximately 50% of human tumors.
    • Cancers with p53 deficiency are frequently characterized by genomic instability, aggressive behavior, and resistance to therapeutic interventions.
    • The p53 gene product regulates multiple DNA damage control pathways and induces cellular senescence.

    Conclusions:

    • The p53 gene is essential for maintaining genomic integrity and preventing malignant transformation.
    • Loss or mutation of p53 function significantly contributes to cancer development and progression.
    • p53 status is a critical factor influencing cancer aggressiveness and treatment outcomes.